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Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-04
A
Akash Saha
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Also affiliated: Winthrop Rockefeller Foundation (2026)
2 h-index
5 pubs
28 cited
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Akash Saha's research focuses on the molecular mechanisms underlying cancer, specifically investigating the role of FAM60A in the Hippo signaling pathway. His recent publication details how the loss of FAM60A disrupts the Sin3/HDAC complex, leading to the activation of YAP1, a key factor in oncogenic processes. This work contributes to understanding how disruptions in protein complexes can promote cancer development. Saha collaborates with researchers at the University of Arkansas for Medical Sciences, including Michael Bauer, Mohammad Alinoor Rahman, Bolni Marius Nagalo, and Md. Rafikul Islam, with whom he has co-authored publications.
Metrics
- h-index: 2
- Publications: 5
- Citations: 28
Selected Publications
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Isolation and molecular characterization of extended-spectrum β-lactamase-producing Escherichia coli and Klebsiella pneumoniae from hospital environments in Northeastern Bangladesh (2026)
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Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)
Collaboration Network
Top Collaborators
Mojnu Miah
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Md Nazmul Huda
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Md Masudul Islam
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Dayebgadoh Gerald
Stowers Institute for Medical Research (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Sneha Khator
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Jahangir Alam
University of Arkansas for Medical Sciences
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Janet L. Thornton
The University of Kansas Cancer Center (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Allen J. Gies
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Michael Bauer
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Kimberly Stephens
University of Arkansas for Medical Sciences
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Bolni Marius Nagalo
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Mohammad A. Rahman
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Michael P. Washburn
The University of Kansas Cancer Center (US)
1 shared publication
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Sayem Miah
Winthrop Rockefeller Foundation
1 shared publication
In database
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
Moshiul Alam Mishu
Shahjalal University of Science and Technology (BD)
1 shared publication
- Isolation and molecular characterization of extended-spectrum β-lactamase-producing Escherichia coli and Klebsiella pneumoniae from hospital environments in Northeastern Bangladesh
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